Pathway 2: Cardiovascular Emergencies
(Adult and Pediatric)
The team continues the resuscitation along the pathway suggested by the initial clinical impression. Each pathway includes a complete, thorough, and rapid physical examination with additional history taking. The team leader is wary of conditions that may not be apparent. To obtain additional clinical data or to correct a missed or newly developed condition, the team leader repeats the initial survey if the patient is not responding satisfactorily.
Please Note: Comments, directions, and instructions specific to pediatric patients are prefaced throughout the manual by PEDS: The pertinent text is underlined.
PEDS: Pediatric considerations. Primary cardiac and vascular emergencies in children are rare. Coronary artery disease, except for in Kawasaki disease, is rare. Congenital heart disease is uncommon, and an emergency case is rare. Cardiac dysrhythmias do occur in children and are discussed wherever appropriate.
Children are not small adults. This needs to be stressed whenever discussing the care of children. Emergency care teams may encounter children needing emergency resuscitation infrequently. The ABCs are still the most important aspect of any resuscitation, but special aspects of the physiology and anatomy of children need to be recognized.
CALS
Initial Approach to Critically Ill or Injured Patients (Vol
I—Acute Care Portals CALS Universal Approach)
Follow
an organized approach to potential serious cardiovascular illness. The
resuscitation team should remain vigilant for possible unrecognized
problems that may make resuscitation difficult or impossible.
Approaching all patients with the CALS Universal Approach helps the
team remain organized and ensures that appropriate resources are
utilized in a systematic manner.
Automated
External Defibrillator (Vol
I—Acute Care Portals Automated External Defibrillator)
When
unresponsive patients are encountered and advanced life support
equipment and/or personnel are not available, activate the 911
emergency system immediately and obtain an automated external
defibrillator (AED), if available. Then check the patient’s pulse and
signs of circulation (breathing, moving, or coughing). If the patient
has no pulse, breathing, or signs of life, initiate CPR with a
compression rate of 100/min, 30 compressions to 2 ventilations. PEDS:
For 2-rescuer
CPR only, administer 15 compressions to 2 ventilations.
As soon as the AED is available:
1. Turn on the AED.
2. Attach the AED electrodes—right upper sternal border and cardiac
apex.
3. Analyze the patient’s rhythm.
4. Follow the directions of the AED and the AED Algorithm.
Advanced Life
Support –
Initial Approach to Cardiac Arrest1
In the setting of a cardiac arrest, follow basic life support protocols until a defibrillator and advanced airway equipment are available. Once the monitor and defibrillator are available, rapidly assess the patient’s rhythm:
- If the patient is in VF/VT, immediately defibrillate. Proceed with the VF/VT protocol if defibrillation is not successful
- If the patient is not in VF/VT, introduce and secure an endotracheal airway, being sure to confirm its proper placement by two methods.
- Follow the appropriate non-VF/VT algorithm: Asystole or PEA (Vol I—Acute Care Portals Asystole; PEA)
- Potential reversible causes for the cardiac arrest must be sought following the 5 Hs and 5 Ts:
| Hypovolemia | Tablets (drug overdose) |
| Hypoxia | Tamponade (cardiac) |
| Hydrogen ion - acidosis | Tension pneumothorax |
| Hyper-/Hypokalemia (or other metabolic) | Thrombosis (coronary) |
| Hypothermia | Thrombosis (pulmonary embolism) |
Ventricular
Fibrillation /
Pulseless Ventricular Tachycardia
(Vol
I—Acute Care
Portals VF/Pulseless VT - Adult and Pediatric; Vol III—CV5 Ventricular Fibrillation/Pulseless Ventricular Tachycardia)
The focus of treating VF/VT is the delivery of early and, as needed, repeated shocks to convert the arrhythmia. This is supported by CPR, advanced airway management and selected medications (as needed). Appropriate use of electricity is the most effective treatment for VF/VT. The earlier the attempted defibrillation shock is delivered after the onset of the VF/VT, the greater the chance of success in converting to a perfusable rhythm. While many drugs are listed as potentially helpful in converting VF/VT, no drug has been classified higher than Class IIb, possibly useful.
Pulseless
Electrical
Activity (PEA) (Vol
III—CV6 Pulseless Electrical Activity)
Pulseless electrical activity (PEA) consists of observing an organized rhythm on the cardiac monitor without a detectable pulse. While the initial approach to the patient consists of basic CPR, advanced airway management, IV access, and frequent IV fluids, the ultimate success depends on the early identification and treatment of a reversible cause for the PEA.
The most frequent reversible
causes are summarized by the 5 Hs and 5 Ts:
| Hypovolemia | Tablets (drug overdose) |
| Hypoxia | Tamponade (cardiac) |
| Hydrogen ion - acidosis | Tension pneumothorax |
| Hyper-/Hypokalemia (or other metabolic) | Thrombosis (coronary) |
| Hypothermia | Thrombosis (pulmonary embolism) |
Asystole (Vol I—Acute Care Portals Asystole - Adult and Pediatric; Vol III—CV7 Asystole)
The initial approach to a patient in asystole consists of CPR, advanced airway management, and IV access. Seek reversible causes of asystole (Hs and Ts), and treat quickly to increase chances of success with the resuscitation. Frequently the asystole is a rhythm consistent with death rather than a treatable condition. The treating team needs to diligently consider if there is evidence that they should NOT be attempting resuscitation—as in situations of DNAR (Do Not Attempt Resuscitation) orders or signs of death. Prolonged attempts at resuscitation of a patient with persistent asystole are rarely indicated except in hypothermia or occasionally with drug overdose.
Patients may present with a wide variety of abnormal rhythms that may have varying degrees of instability or risk of deteriorating into an unstable condition (CHF, shock, hypoxia, acute coronary syndrome) or into a full cardiac arrest. Many associated clinical conditions influence the potential seriousness of the arrhythmias and the aggressiveness needed in the treatment. Some of these associated conditions that increase the risk include: the age of the patient (especially the elderly), the presence of an impaired heart (ejection fraction of the left ventricle < 40%), electrolyte abnormalities (hypokalemia, hyperkalemia, hypocalcemia, hypercalcemia), hypoxia, acidosis, hyperthyroidism, drug over-dose (tricyclic antidepressants), or cocaine use. Frequently the most appropriate treatment of the arrhythmia necessitates the search for and treatment of the associated aggregating conditions.
Bradycardia (Vol I—Acute Care Portals Bradycardia - Adult and Pediatric; Vol III—CV10 Bradycardia)
Key points when evaluating a patient with bradycardia:
- Treat the patient, not the monitor.
- A heart rate of 65 may be a relative bradycardia if the patient’s BP is low.
- Consider the normal range of vital signs in pediatric patients.
| PEDS: Normal Pediatric Vital Sign Ranges2,3 | |||
Normal RR |
Normal HR | Systolic BP (lower limit) | |
| Newborn (2 kg) | 30 to 60 | 100 to 190 | >45 |
| Newborn (4 kg) | 30 to 60 | 100 to 190 | >60 |
| Infant (<1 yr) | 30 to 60 | 80 to 160 | >60 (or strong pulses) |
| Toddler (1 to 3 y) | 24 to 40 | 80 to 150 | >70 (or strong pulses) |
| Preschool (4 to 5 y) | 22 to 34 | 80 to 140 | >75 |
| School age (6 to 12 y) | 18 to 30 | 70 to 120 | >80 |
| Adolescent (12 to 20 y) | 12 to 20 | 60 to 100 | >90 |
- Look for signs (such as decreased LOC, hypotension, or CHF) and symptoms (such as chest pain or shortness of breath) that indicate adverse clinical manifestations associated with the bradycardia.
- Make sure that the patient’s signs and symptoms are due to the slow heart rate. Shock from any cause, hypovolemia, hypoxia, or myocardial dysfunction may cause hypotension associated with a bradycardia (or a relative bradycardia for the situation), but the patient may not have primary cardiac conduction system abnormality or primary autonomic cause for the bradycardia.
Key Points to Remember in Treating Bradycardia
- If the patient has a bradycardia or heart block and has signs and symptoms from this bradycardia, initiate and perform treatment quickly and decisively.
- These patients' conditions may be pre-cardiac arrest and merit aggressive intervention, including a number of interventions together, such as transcutaneous pacing, atropine IV, and preparation for an epinephrine infusion.
- In a symptomatic patient, give atropine 0.5 mg IV to a maximum dose of 0.03 to 0.04 mg/kg with dosing intervals of 3 to 5 minutes. The severity of the patient's symptoms determines the interval of dosing. Thus, use the 3-minute dosing interval in severe clinical situations. PEDS: Use epinephrine 0.01 mg/kg (0.1 mL/kg of a 1:10 000 solution) IV/IO. In children, bradycardias < 60 with poor perfusion are an indication for CPR.
- Dopamine IV starting at rates of 2 μg/kg/min may be given and increased rapidly up to 10 μg/kg/min. Or epinephrine drip 2 to 10 μg /min may be used to increase the heart rate and blood pressure if other measures are ineffective.
- In patients with severe signs and symptoms from the bradycardia, consider the immediate use of transcutaneous pacing. Do not wait for IV access or for the atropine to become effective.
- Transcutaneous pacing may be effective but painful, and the patient may need sedation.
- Hypovolemia or myocardial dysfunction may cause bradycardia and need to be treated.
- The prognosis in AV block is related to the site of the infarction (anterior vs. inferior), the site of the block (intranodal [proximal or above the His Bundle] or infranodal [distal or below the His Bundle]), the nature of the escape rhythm, and the hemodynamic consequences.
- Transplanted (denervated) hearts do not respond to atropine. The treatment of symptomatic bradycardia in these patients requires catecholamine infusion, pacing, or both.
Transcutaneous
Pacing (Vol
III—CV10 Bradycardia)
Transcutaneous pacing (TCP) is a Class I intervention for all symptomatic bradycardia. It is especially useful when other forms of treatment of the bradycardia are either ineffective or will take too long to implement such that the patient becomes progressively unstable. To be effective, TCP must be begun as early as possible in the treatment sequence before the patient develops severe hypoxia or acidosis.
Indications for TCP
- Treatment of hemodynamic significant bradycardia that has not responded to atropine or epinephrine.
- TCP is useful as a short interval bridge until transvenous pacing can be initiated.
- TCP can be a bridge until bradyarrhythmias from hyperkalemia or drug overdose can be reversed.
- TCP is useful when the patient has received or will receive thrombolytic therapy, and therefore, vascular puncture for transvenous pacing is undesirable.
Technique of TCP
- Anterior/posterior application. Place an anterior pacing pad to the left of the sternum centered as close as possible to the point of the maximum cardiac impulse. Place the posterior pad directly behind the anterior pad to the left of the thoracic spine column. An alternative placement would be a sternum-apex position.
- Sternal-apex chest wall pad placement includes one pad in the right upper chest and a second pad on the left lateral chest wall.
- Place regular 3- or 4-lead ECG electrodes for monitoring the underlying rhythm.
- Initiate TCP at a rate of 60 to 70 bpm.
- Initial output from the pacer in the case of bradysystolic arrest should be maximum output, which is 200 mA. With a non-arrest bradycardia, start at a lower power setting and slowly increase the output until achieving capture. Electrical capture usually requires 50 mA to 100 mA.
- Determination of capture may be difficult on a routine monitor because of the wide electrical activity obliterating the cardiac electrical activity on the monitor. A filter is on the pacing monitor, such that capture can usually be determined. Capture also can be assessed by BP determination. If a peripheral pulse is to be obtained, obtain it at the right carotid or right femoral artery, so as not to confuse the jerking of muscle contraction with that of a pulse.
- CPR may be administered directly over the insulated pacing pads while pacing is going on, without risk to the CPR operator.
- Capture success and energy levels are related to pad placement, patient size, and body size. Large pericardial effusions may inhibit capture.
- TCP is painful, and the patient needs analgesia in the form of narcotics and/or sedation with a benzodiazepine.
Pitfalls of TCP
- Failure to recognize the presence of underlying treatable VF
- Failure to recognize that the pacemaker is not capturing
- Induction of arrhythmia, such as VF
- Skin damage due to prolonged pacing
Tachycardia (Vol
I—Acute Care PortalsTachycardia Overview; Vol III—CV8 Tachycardia)
Key Points when Evaluating a Patient with Tachycardia
- Does the patient have signs and symptoms (such as shock, pulmonary edema, CHF, chest pain, or decreased LOC) associated with the tachycardia?
- Are the patient’s signs and symptoms a result of the patient’s tachycardia or does the patient have a serious underlying condition (such as septic shock or hypovolemia) that is causing an appropriate sinus tachycardia? Heart rates < 150 bpm usually do not cause serious signs and symptoms unless the tachycardia continues for a prolonged period of time.
- Is the tachycardia causing such serious signs or symptoms that the patient must be immediately cardioverted, or can the patient's tachycardia be evaluated and considered for treatment with medications?
- What is the safest way to treat the patient’s tachycardia? All antiarrhythmic medications may cause a proarrhythmic effect, regardless of their Vaughn-Williams classification. The use of more than one antiarrhythmic in the same patient exponentially increases the risk of side effects.
- What is the patient’s specific rhythm that is causing the
tachycardia?
- Is the rhythm sinus tachycardia? If so, determine the cause of the sinus tachycardia and treat the underlying cause.
- Is the basic rhythm atrial flutter or atrial fibrillation?
- Is the narrow complex supraventricular tachycardia due to abnormal automaticity as in ectopic atrial tachycardia or multifocal atrial tachycardia (MAT) or due to re-entrant circuits as in AV nodal re-entrant tachycardia (AVNRT) or AV re-entry tachycardia (AVRT)?
- Is the tachycardia of supraventricular or ventricular origin? Treat a wide complex tachycardia as ventricular tachycardia until proven otherwise.
- Does the patient have an accessory AV pathway as seen in Wolff-Parkinson-White (WPW) syndrome?
- If the patient is in ventricular tachycardia, is the ventricular tachycardia monomorphic or polymorphic?
- If the ventricular tachycardia is polymorphic, is it associated with a prolonged baseline QT interval or represent torsades de pointes?
- Is the patient’s left ventricular function significantly impaired (ejection fraction < 40% or signs of CHF)? Antiarrhythmic medications must be used with caution in patients with depressed left ventricular function or overt CHF. Many of the antiarrhythmic medications further depress the left ventricular function and thus worsen or precipitate CHF. Amiodarone is now often the first agent to be used to treat tachycardias due to its lesser negative inotropic effect and its broad antiarrhythmic activity. In many situations, if amiodarone fails to control the tachycardia, early electrical cardioversion should be the next intervention.
- Does the patient have an identifiable cause for the arrhythmia such as hypokalemia, hypoxia, acute MI, or CHF?
Atrial
Fibrillation – Atrial Flutter (Vol I—Acute Care Portals Atrial Fibrillation/Atrial Flutter - Adult; Vol III—CV8 Tachycardia)
For patients with atrial fibrillation/atrial flutter, the clinician must first assess whether the patient is hemodynamically unstable and experiencing serious signs and symptoms (ie, hypotension, angina) from a rapid ventricular rate. If serious signs and symptoms are present, immediate electrical cardioversion is necessary, regardless of the duration of the atrial fibrillation/flutter (Class I).
The initial evaluation of the hemodynamically stable patient with atrial fibrillation/atrial flutter must answer four questions before definitive treatment is begun. These include:
- Is there an underlying reversible cause for the AF? Acute medical conditions that might cause atrial fibrillation/flutter include hypoxia, CHF, hypokalemia, hypertension, anemia, hypomagnesemia, mitral regurgitation, acute MI, digoxin toxicity, or thyrotoxicosis. If one or more of these are present, they must be treated as part of the AF management.
- Is the cardiac function impaired? Patients with symptomatic CHF or an ejection fraction < 40% require special precautions to be taken when medications are used to treat the AF. Many antiarrhythmic medications have negative inotropic and proarrhythmic properties that manifest in patients with an ejection fraction < 40%.
- Does the patient have Wolff-Parkinson-White (WPW) syndrome? Patients with WPW have an accessory conduction pathway between the atria and the ventricle. Many antiarrhythmic medications have the potential of causing a paradoxical increase in the ventricular rate in patients with WPW.
- Has the patient been in AF for less than or greater than 48 hours? If the patient has been in AF for greater than 48 hours, there is an increased risk of clot formation in the atria and systemic embolization with conversion to sinus rhythm. If stable, the patient requires rate control and anticoagulation for 3 weeks prior to cardioversion.
The management of a patient with hemodynamically stable atrial fibrillation/atrial flutter consists of three primary focuses:
- The control of the ventricular rate.
- The determination of the need for anticoagulation.
- The conversion of the atrial fibrillation/atrial flutter to sinus rhythm.
Narrow Complex Supraventricular Tachycardia
(Vol I—Acute Care Portals Tachycardia Overview;
Vol III—CV8 Tachycardia)
Narrow Complex Supraventricular Tachycardias include:
- Paroxysmal supraventricular tachycardia (PSVT) caused by a re-entrant circuit, as in AV nodal re-entrant tachycardia (AVNRT) or AV re-entry tachycardia (AVRT).
- Automatic atrial tachycardia caused by abnormal automaticity in the atria, as in ectopic atrial tachycardia or multifocal atrial tachycardia (MAT).
- Junctional tachycardia (rare).
While the
mechanism causing the tachycardia helps to dictate the most appropriate
treatment, frequently the mechanism of the arrhythmia may be difficult
to determine. Nevertheless, since the therapeutic approach is different
for PSVT vs automatic atrial tachycardia vs junctional tachycardia, it
is important that a specific diagnosis be established. The following
diagnostic tools may help in this differential:
- Evaluation of the 12-lead ECG with special attention to the P-waves. Ectopic atrial tachycardia has abnormal P-wave configuration and P-wave axis. MAT is irregular like atrial fibrillation but has three or more different P-wave morphologies identifiable preceding the QRS complexes.
- Clinical information may also help in the differentiation. PSVT tends to have an abrupt onset and termination, while the automatic atrial tachycardias tend to start and stop more gradually. Many patients with PSVT have previously been diagnosed as having PSVT or an accessory pathway.
- The initial use of vagal maneuvers can also help to differentiate the type of the tachycardia. Vagal maneuvers cause slowing of conduction through the AV node by an increase in parasympathetic tone. The simplest vagal maneuver is the Valsalva (bearing-down) maneuver. Other vagal maneuvers that may be tried include coughing, induction of the gag reflex, or facial immersion in ice water.
- Adenosine IV may also be helpful (provided that there are no contraindications) both in differentiating the type of tachycardia (ie, making the P-waves evident) and possibly in terminating the tachycardia. Remember that adenosine must be used with great caution, if at all, in patients with reactive airway disease because it may precipitate bronchospasm.
Regular Wide
Complex Tachycardia (Vol
I—Acute Care Portals Tachycardia Overview; Vol III—CV8 Tachycardia)
The treatment of patients with regular wide complex tachycardia may be controversial. The accuracy of determining if the tachycardia is ventricular versus supraventricular with aberrant conduction based on ECG criteria is often unreliable. Giving verapamil or diltiazem to a patient with VT may cause hemodynamic collapse. Therefore, treat wide complex tachycardia as if it is VT, unless the team is absolutely certain that the rhythm is PSVT. Most cases of wide complex tachycardia are of ventricular origin.
The initial approach to wide complex tachycardia is to determine if the patient is hemodynamically stable. If the patient is hemodynamically unstable due to the tachycardia (altered LOC, CHF, impaired tissue perfusion), perform immediate electrical cardioversion.
In hemodynamically stable patients, attempt to distinguish if the patient has stable ventricular tachycardia or supraventricular tachycardia with aberrancy. Useful clues to help make this decision include:
-
If the patient has a history of coronary artery disease or other structural heart disease, the rhythm is more likely to be ventricular in origin.
-
A history of aberrant rhythms, preexisting bundle branch blocks (BBB) or rate-dependent BBB, or accessory pathways suggests supraventricular tachycardia with aberrancy if the QRS from the previous ECG matches that observed with the tachycardia.
-
Carefully evaluate a 12-lead ECG for AV dissociation. The loss of the normal 1:1 association between P-waves and QRS complexes is a reliable criterion of ventricular tachycardia.
-
Administration of adenosine may be considered in order to identify and treat a suspected aberrant SVT.
If you are able to make a specific diagnosis of the wide complex tachycardia, follow the appropriate algorithm that matches the diagnosis.
Ventricular
Tachycardia (Vol
I—Acute Care Portals Tachycardia Overview; Vol III—CV8 Tachycardia)
Although it is often difficult to be sure if a wide complex tachycardia is VT or not, some clues help in making this determination. Some features that suggest ventricular tachycardia include:
-
Presence of AV dissociation
-
Fusion/capture beats
-
Left axis deviation in the frontal plane on the 12-lead ECG
-
QRS width > 140 ms
-
Clinical history of coronary artery disease
Key Approaches to Patients with Ventricular Tachycardia
- The approach to patients assumed to be in VT is largely determined by the hemodynamic stability of the patient. Patients with VT who are in full cardiac arrest are treated the same as patients in VF. (Vol III—CV5 Ventricular Fibrillation/Pulseless Ventricular Tachycardia) Patients with VT who have a pulse but are hemodynamically unstable must be immediately cardioverted. (Vol III CV5 Ventricular Fibrillation/Pulseless Ventricular Tachycardia)
- In hemodynamically stable ventricular tachycardia, the form of the VT needs to be differentiated between monomorphic VT and polymorphic VT.
- Monomorphic VT has QRS complexes that are fairly uniform from beat to beat. In the treatment of monomorphic VT, it is beneficial to know if the patient has a left ventricular hypertrophy with reduced function (ejection fraction <40% or CHF) or normal function (ejection fraction >40%) to help decide on the most appropriate drug therapy.
- In polymorphic VT, the QRS morphology varies, is irregular in rate and is more unstable, and thus more likely to degenerate into ventricular fibrillation. The polymorphic VT may be found in the setting of a normal baseline QT interval (no evidence of torsades de pointes) or it may be associated with a prolonged baseline QT interval (where torsades de pointes is more common). Torsades de pointes is a special form of polymorphic VT with a characteristic ECG appearance described as twisting of the points. This form of VT is seen especially in patients with a prolonged QT interval. Torsades de pointes is often associated with hypomagnesemia, hypokalemia, use of many antiarrhythmic drugs, and tricyclic agents. The recognition of torsades de pointes is important because the treatment approach is different from the usual uniform morphology VT. If the patient is unstable hemodynamically, immediate defibrillation needs to be used to attempt conversion. Defibrillation is frequently not successful in converting the torsades de pointes to a normal rhythm; thus, medications (such as magnesium sulfate given at a dose of 1 to 2 g IV over 1 to 2 minutes) and/or overdrive pacing will be needed to attempt to convert this difficult rhythm.
Long QT
Syndrome
(LQTS) (Vol III
CV15 Long QT Syndrome)
The long QT syndrome (LQTS) represents a diverse group of disorders that can be inherited (the genetic form) or acquired. The inherited cases are caused either by the more common autosomal dominant Romano-Ward type or the rare autosomal recessive Jervell and Lange Nielsen type that is associated with congenital deafness. These genetic mutations encode for abnormal cardiac ion channels. The acquired forms are caused by a large number of stimuli. The most common causative agents are the Class I and Class III antiarrhythmic agents, but many other drugs and conditions are known to increase the risk of prolonging the QT interval. One important distinction between the inherited and the acquired forms of LQTS is that correcting the underlying disorder or discontinuing the offending drug can often reverse the acquired form. All patients with the LQTS share a prolongation of the QT interval. This is associated with an increased risk of developing a specific type of polymorphic ventricular tachycardia called torsades de pointes or “twisting of points.”
Symptoms Related
to LQTS
Many people with a
LQTS live for many years without any symptoms from their LQTS, but when
symptoms do occur they are often serious. The most common symptoms are
syncope or sudden death, typically occurring during physical activity
or emotional upset. The most common age to see the symptoms is in the
preteen to teenage years, but the symptoms may first appear from the
first days of life to middle age. Sudden and unexplained loss of
consciousness or cardiac arrest in a child or teenager or a family
history of unexplained syncope or sudden death in a young person should
raise the suspicion of LQTS.
PEDS: Tachycardia in Infants
or Small Children
| PEDS: Normal Pediatric Vital Sign Ranges2,3 | |||
| Normal RR | Normal HR | Systolic BP (lower limit) | |
| Newborn (2 kg) | 30 to 60 | 100 to 190 | >45 |
| Newborn (4 kg) | 30 to 60 | 100 to 190 | >60 |
| Infant (<1 yr) | 30 to 60 | 80 to 160 | >60 (or strong pulses) |
| Toddler (1 to 3 y) | 24 to 40 | 80 to 150 | >70 (or strong pulses) |
| Preschool (4 to 5 y) | 22 to 34 | 80 to 140 | >75 |
| School age (6 to 12 y) | 18 to 30 | 70 to 120 | >80 |
| Adolescent (12 to 20 y) | 12 to 20 | 60 to 100 | >90 |
Decompensation in small children with tachycardia is usually an effect of sepsis, fever, and shock from other causes, rather than from the tachycardia. Sinus tachycardia responds to treatment of the underlying cause.
Extreme sinus tachycardia may be difficult to differentiate from SVT because the rates may be similar. The following points can help to distinguish between them:
- Heart rate. Sinus tachycardia is usually at a rate < 200 bpm. The rate in SVT is usually > 230 bpm, but there is overlap.
- ECG. P waves may be difficult to see when the heart rate is more than 200 bpm. If the P waves can be seen, they usually have an abnormal axis in SVT.
- Variability. In sinus tachycardia there may be beat-to-beat variation in rate.
SVT in small children is most often caused by a re-entry mechanism involving an accessory pathway of the AV conduction system.
As opposed to adults, most children tolerate SVT well. If SVT results in shock, it must be reversed emergently.
The heart rate associated with SVT varies according to the child’s age. In infants, the rate is commonly 240 bpm. The rate is regular. At very high rates, P waves may not be seen. The QRS duration is usually normal, although a wide QRS can be seen. Distinguishing SVT from VT, AF, and atrial flutter may be difficult. However, treat all of these dysrhythmias in an unstable child with synchronized cardioversion.
Perform synchronized cardioversion without delay for a child in shock. Use an initial setting of 0.5 to 1.0 J/kg. Ideally, intubate and oxygenate the patient prior to synchronized cardioversion.
Attempt vagal maneuvers in stable patients. Place a washcloth soaked in ice water on the patient’s face for no longer than 30 seconds. This may be repeated.
Older children can perform a Valsalva’s maneuver.
Adenosine 0.1 mg/kg rapid IV push with constant ECG monitoring produces a transient AV block that interrupts the re-entrant circuit. If the first dose fails, it may be repeated once at twice the dose (not to exceed 12 mg). Use adenosine when the patient is stable enough to allow time to start an IV.
Cardioversion (Vol
I—Acute Care Portals Electrical Cardioversion - Adult and Pediatric; Vol III—CV9 Electrical Cardioversion)
Strongly consider cardioversion early in the treatment of patients whose tachycardia (usually with ventricular rates > 150) is causing serious hemodynamic effects and when administration of medication is either ineffective, contraindicated, or has too slow an onset of action to correct the tachycardia. Signs and symptoms of CHF—decreased LOC, hypotension/shock, or persistent chest pain—are some of the patient findings that should prompt a team to consider electrical cardioversion. Determine whether the serious signs and symptoms are due to the tachycardia rather than the tachycardia being a response to another condition, such as hypovolemic shock or pain. This is crucial.
The resuscitation team performs many actions (team action) almost simultaneously in preparation for synchronized cardioversion. The team must remember that the seriousness of the patient's signs and symptoms determines how quickly the cardioversion must be accomplished to prevent deterioration in the patient's hemodynamic condition.
Note that cardioversion is a very unpleasant experience, and most alert patients require intravenous sedation. Be prepared to manage the airway in a sedated patient.
There are numerous potential causes (both cardiac and non-cardiac in origin) for chest pain. The urgency of dealing with chest pain is determined by making a correct working diagnosis for the cause.
Cardiovascular
etiologies for chest pain
| Acute myocardial infarction | Pericarditis |
| Dissection of the thoracic aorta | Stable or unstable angina |
| Hypertensive crisis | Pulmonary embolus |
| Arrhythmias
(significant bradycardia or tachycardia) |
Non-cardiovascular etiologies for chest pain
| Costochondritis | Pneumothorax |
| Cholecystitis | Pneumonia/pleurisy |
| Esophagitis/spasm- gastroesophageal reflux disease (GERD) |
Chest trauma |
Acute Coronary
Syndrome (Vol
III—CV11 Acute Coronary Syndrome)
The term acute coronary syndromes (ACS) describes a spectrum of clinical diseases that includes Q-wave myocardial infarction (which generally presents with ST-segment elevation), non-Q-wave myocardial infarction (which generally presents without ST–segment elevation), and unstable angina. These patients all have in common the disruption by fissuring or erosion of a lipid-rich plaque.
CALS Approach to
Patients with Suspected Acute Ischemic Chest Pain:
Complete the following within the first 10 minutes of the patient’s
arrival:
- Obtain vital signs, including oxygen saturation.
- Deliver appropriate oxygen.
- Attach cardiac monitor and observe initial rhythm; determine whether to treat the rhythm immediately.
- Obtain IV access, including venous blood for initial blood studies.
After the preceding initial steps, continue the rapid evaluation of the patient with chest pain by performing or ordering the following:
- Complete the targeted SAMPLE history. This may include getting information from prehospital care providers, friends, or relatives.
- PQRST is a good assessment tool to obtain information regarding the chest pain. P-What provokes the pain? What was the patient doing when the pain presented? Q-What is the quality of the pain? R-Does the pain radiate? What relieves the pain? S-How severe is the pain? T-What time did the pain start?
- Relay all information to the team leader. This information may be critical to initial patient management and determination of fibrinolytic use.
- Perform a focused physical examination and specifically determine
the patient’s eligibility for fibrinolytic therapy.
- Obtain a 12-lead ECG.
- Assess the initial 12-lead ECG, history, and information from the focused physical examination to determine if the patient is an appropriate candidate for acute reperfusion with either fibrinolytic therapy or percutaneous coronary intervention (PCI, ie, angioplasty and/or stenting).
- Obtain the initial laboratory and x-ray tests. A pre-set battery of venous blood studies for acute coronary syndrome (including initial cardiac marker levels, electrolytes, CBC, and coagulation studies) may facilitate the laboratory evaluation.
- Consider the need for a chest x-ray.
- From the preceding, the team develops a preliminary impression.
Initial Treatment
Although
many treatment protocols may be used simultaneously, for immediate
treatment of a patient suspected of having chest pain of ischemic
origin, have four drugs readily available: oxygen, aspirin,
nitroglycerin, and morphine.
Quickly weigh the risks and benefits of each. The American Heart Association1 recommends the memory aid “MONA greets all patients.”
Oxygen at a rate of at least 4 L/min
Aspirin 160 to 325 mg, if not contraindicated (Chewing speeds absorption.)
Nitroglycerin SL or as a spray as many as 3 times, as long as not contraindicated by hypotension, suspected right ventricular infarction, or the patient’s use of phosphodiesterase-inhibitor medications (eg, Sildenafil (Viagra) within a time period specific to each drug in this class. (If nitroglycerin does not fully relieve the pain, use morphine IV.)
Morphine sulfate 1 to 3 mg IV, repeated as needed, with the goal to render the patient pain-free. (Be careful in patients with hypotension [especially hypovolemia of right ventricular infarction] or bradycardia.)
The treatments that follow must be individualized to the specific patient needs, laboratory findings, clinical setting, and resources available. Some treatment choices include:
-
The need for reperfusion therapy – either by fibrinolytics or angioplasty
-
The need for anticoagulation therapy with such agents as heparin or IIb/IIIa agents or clopidogrel
-
The need for beta blocker therapy
-
The need for ACE inhibitor therapy
-
The need for management of arrhythmias
-
The need for invasive intervention, such as performing a diagnostic angiogram, angioplasty, or coronary artery bypass graft
-
The need to manage complications of the acute coronary syndrome, such as CHF or shock
Hypotension –
Shock (Vol
III—Trau Care 2 Shock)
Severe hypotension and shock can be due to a wide range of causes exhibited in a variety of ways. All shock states are characterized by inadequate cellular perfusion and oxygen delivery to cells to maintain adequate metabolic function. Shock states can manifest in a wide variety of ways, based in part on their cause and in part on the compensatory mechanism on the patient. However, all shock states result in tissue hypoperfusion, tissue injury, and ultimate tissue damage.
One way of defining the cause of shock is to consider the potential broad physiological categories that can result in shock:
- Cardiac rate problem – heart rate either too slow or too fast to meet the metabolic needs of the body
- Volume problem
– due to an absolute or relative vascular volume
deficiency.
- Vascular volume loss as from hemorrhage or dehydration
- Distribution problem due to vasodilatation or third space fluid loss as in spinal shock, anaphylaxis, or septic shock
- Pump problem – left ventricular failure due to primary heart abnormalities resulting in inadequate cardiac output
- Inadequate preload – due to obstruction or lack of proper filling of the right ventricle of the heart as occurs with tension pneumothorax, cardiac tamponade, large pulmonary emboli, or right ventricular infarction
Consider the mnemonic SHRIMPCAN to help develop a broad differential if the cause is still unknown:
| S | Sepsis—gram-negative infection or other overwhelming infection |
| H | Hypovolemia resulting from hemorrhage, dehydration, vomiting, peritonitis, pancreatitis, leaking aneurysm, ectopic pregnancy |
| R | Respiratory compromise resulting in hypoxia, tension pneumothorax, massive pulmonary embolus |
| I | Ingestion of a toxic substance, drug overdose |
| M | Metabolic causes including diabetic ketoacidosis, hyperosmolar coma, myxedema, adrenal insufficiency, electrolyte abnormalities |
| P | Psychiatric causes such as water intoxication |
| C | Cardiogenic shock, acute myocardial infarction, cardiomyopathy, cardiac tamponade, dysrhythmias, severe cardiac failure, valvular heart disease, atrial myxomas |
| A | Anaphylactic shock |
| N | Neurogenic causes such as spinal shock, herniation syndromes, intracranial bleed |
Congestive
Heart
Failure/Pulmonary Edema (Vol
III—CV12 Acute Heart Failure)
Patients with severe CHF and/or pulmonary edema may exhibit varying degrees of pulmonary congestion, such as tachypnea, labored breathing, rales, jugular venous distention, frothy sputum, and cyanosis. In addition, the reduced cardiac output may result in weak pulses, pallor, diaphoresis, and hypotension. If the cause for the severe congestive heart failure (such as severe bardycardia or tachycardia) can be identified, treat aggressively.
Initial
Management
-
Administer oxygen while attaching the patient to the ECG monitor, oxygen saturation, obtaining a rhythm strip and patient vitals.
-
Alert patients may benefit from CPAP or BiPAP.
-
Establish IV access.
-
Give nitroglycerine SL to reduce preload if systolic blood pressure is greater than 100 torr.
-
Other useful medications include ACE inhibitors, nesiritide, dobutamine, inamrinone, and imrinone. (Vol III CV12 Acute Heart Failure)
-
Consider administering morphine 2 to 5 mg IV to assist with peripheral dilation to decrease preload and help relieve anxiety. This helps to decrease oxygen demands.
-
Assist ventilation as necessary; early intubation with the use of RSI may be lifesaving.
-
If the patient is normotensive or hypertensive, start a nitroglycerine drip at 10 to 20 μg/min and titrate blood pressure down to a systolic blood pressure of 100 torr. If the initial blood pressure was high, titrate until the mean blood pressure is 30% lower than on arrival.
-
If signs of fluid overload are present, administer Lasix 40 to 100 mg IV.
Patients with severe cardiomyopathy can present in cardiac arrest or severe CHF (cardiogenic shock). The cardiomyopathy may be due to end-stage CHF, arteriosclerotic heart diseases, chronic alcoholism, or a wide range of other causes. Such patients who can be stabilized should be considered for intra-aortic balloon pumping as a bridge to heart transplant or other therapy.
Digitalis
Toxicity (Vol
III—CV14 Digitalis Toxicity)
Digoxin is the form of cardiac glycoside used clinically as part of the management of CHF and to assist in slowing ventricular heart rate in patients with atrial fibrillation. Clinical manifestations of digitalis toxicity include gastrointestinal and neurologic symptoms along with a wide variety of cardiac arrhythmias.
Initial Management
- The most important element of successful treatment of digitalis toxicity is early recognition of the patient’s symptoms and/or arrhythmias related to digitalis toxicity. Temporary withdrawal of the drug along with ECG monitoring (if indicated) often suffices for treatment.
- Potassium replacement is indicated for patients with hypokalemia or when serum potassium levels are in the low normal range. This is particularly useful if the patient has an ectopic tachyarrhythmia. Potassium replacement must be used cautiously in patients with conduction disturbance since the atrial ventricular conduction may be further slowed by rapid replenishment of serum potassium.
- Significant arrhythmias need to be carefully managed.
- Digitalis-specific antibody therapy (Digibind or FAB fragment therapy) may be considered in severe digitalis toxicity.
Hypertensive
Crises (Vol
III—CV13 Hypertensive Crises)
Hypertension emergencies are those situations that require immediate reduction of the blood pressure (not necessarily to normal) to prevent or limit target organ damage. Examples include severe hypertension associated with encephalopathy, intracranial hemorrhage, acute left ventricular failure with pulmonary edema, aortic dissection, eclampsia or severe pregnancy-induced hypertension, unstable angina, or acute myocardial infarction. Hypertensive urgencies are those situations in which it is desirable to lower the blood pressure within 24 hours. Examples include accelerated or malignant hypertension without symptoms or progressive target organ complications and situations where severe post-operative hypertension occurs.
Initial Management
- Rapid blood pressure reduction to normal may cause cerebral hypoperfusion.
- The goal of treatment is to reduce the mean arterial pressure by 20% to 25% over a period of minutes to hours.
- Most patients are volume depleted, probably due to pressure-induced diuresis.
- Diuretics and fluid restriction should be reserved for patients who are clinically fluid overloaded.
Dissection of the thoracic aorta occurs when the pulsatile flow of blood breaks through the intimal lining of the aorta into the media of the vessel wall. The arterial blood then separates the intima from the media and adventitia and travels up and down the wall of the aorta. This defect may be caused by arteriosclerosis and hypertension or a congenital weakness of the aortic wall. Patients (tall and thin) with Marfan’s syndrome are at an increased risk for the disorder.
The typical dissection patient presents with tearing chest pain. If the dissection mainly involves the ascending aorta, the pain is mainly anterior. If the dissection begins in the distal arch, the pain is mainly between the shoulder blades. The pain begins suddenly and tends to occur in males with a history of hypertension.
When the dissection begins in the ascending aorta, distortion of the aortic valve may occur with valvular incompetence. The left coronary artery may become occluded. Frequently, the dissection will rupture into the pericardial sac, producing hemopericardium and tamponade. The dissection can involve the carotid arteries, producing stroke signs. The origin of the left subclavian artery can be involved, resulting in a diminished blood pressure in the left arm as compared to the right.
When the dissection begins more distally, it may dissect into the abdominal aorta and may involve the femoral arteries. Renal arteries and splanchnic arteries may be compromised. Pulses may become reduced in the femoral arteries.
The differential diagnosis includes acute myocardial infarction, so be careful to consider thoracic aortic dissection in the patient who may receive thrombolytic therapy or heparinization.
Initial Management
- The chest x-ray is seldom diagnostic in establishing the diagnosis. CT of the aorta with IV contrast is the most common diagnostic modality. Trans-esophageal echocardiography if available is also diagnostic. Ultrasound may be helpful in picking up hemopericardium and tamponade. If such is found, placement of an indwelling catheter may allow intermittent decompression to buy time until surgical correction is possible. (Vol II—Circ Skills 8 Saphenous Vein Cutdown)
- Treatment involves decreasing the pulsatile effect of cardiac contraction while also blocking peripheral alpha-adrenergic effects. The alpha and beta blocker, labetalol (Normodyne, Trandate) 20 mg IV every 10 min up to 300 mg accomplishes both of these effects. The effect of the labetalol lasts several hours.
- Target a systolic blood pressure of about 80 to 100 torr. You may continue an infusion of 2 mg/min. Labetalol is contraindicated in CHF, heart block, and reactive airway disease.
- If the dissection is in the ascending aorta or results in the occlusion of major branches of the aorta, emergency surgery may be needed. Obtain early consultation.
Distended neck veins, hypotension, and muffled heart sounds comprise Beck’s triad of signs of cardiac tamponade. Unfortunately, these signs are not always present.
Cardiac tamponade may have resulted from myocardial rupture secondary to a myocardial infarction several days previous. Such cases may be salvageable because the site of rupture is usually the thick free wall of the left ventricle and the opening is usually small and repairable.
Cardiac tamponade may also have resulted from dissection of the thoracic aorta with rupture into the pericardial sac, effusion secondary to myocarditis or pneumonia, chest trauma, or (PEDS) pericarditis in a child.
Initial Management
- Use ultrasound through a subxiphoid window to make the diagnosis whenever the possibility arises. (Vol III—UL2 Emergency Ultrasound Techniques) Alternatively, perform a diagnostic pericardiocentesis. (Vol II—Circ Skills 6 Pericardiocentesis) When significant symptomatic cardiac tamponade is found, place a catheter in the pericardial sac to intermittently decompress the pericardial sac until the patient can be taken to surgery. This tamponade associated with a thoracic aorta dissection is also amenable to surgery if the patient can be stabilized with repeated aspiration and an alpha and beta blocker (labetalol) used to minimize further dissection. (See Thoracic Aorta Dissection, #25 this pathway)
Tension
Pneumothorax Vol I—Pathway 6, Adult Respiratory)
The emergency treatment of tension pneumothorax is addressed in Vol II—Breath Skills 5 Needle Thoracostomy.
The emergency treatment of pulmonary embolism is addressed in Vol I, Pathway 6 Adult Respiratory, #10.
Air Embolism
In any patient with a right to left shunt, air embolism is a great danger. Normal patients tolerate small bubbles of air in IV lines without a problem. These small bubbles are trapped in the lungs where they are gradually dissolved by the blood. In shunt patients, the bubbles can cross through the shunt into the arterial tree. They can lodge in the brain or heart and cause serious problems.
Initial Management
- Place the patient who has air embolism on his or her left side in an attempt to keep the air in the right heart. Place the patient in steep Trendelenburg position to lessen the probability of cerebral embolism.
- Insert a central venous line to aspirate air from the right atrium and ventricle if the crunching sound of Hamman can be heard over the precordium. Seizures are common and can be resistant to treatment. Hyperbaric oxygenation is the treatment of choice for air embolism.
Leaking
Abdominal Aortic
Aneurysm (AAA)
The emergency treatment of leading abdominal aortic aneurysm (AAA) is addressed in Vol I, Pathway 3 Gastrointestinal/Abdominal Emergencies, #6.
Implanted
Cardioverter-Defibrillator (ICD)
If you are touching a patient as the patient’s ICD discharges, you will feel a shock, but you will not be endangered.
Initial Management
- Avoid placing pacing or defibrillator paddles/pads directly over the implanted device. Otherwise, in all emergencies other than ICD-related problems, treat the patient as if an ICD were not present.
- Consult the patient’s cardiologist regarding management of the ICD post-resuscitation.
- If an ICD is firing erratically, disarm the ICD by placing a magnet on the skin over the subcutaneous pulse generator. Response will vary with ICD type, but most devices will be disabled as long as the magnet remains on the pulse generator. Magnets designed for disabling pacemakers and ICDs should be available in all emergency departments.
Congenital and
Acquired
Heart Defects (Tetralogy of Fallot, Valvular
Heart Defects)
Tetralogy of Fallot
Fortunately, most congenital heart defects rarely present as emergencies. PEDS: Children with right to left shunt heart defects (such as tetralogy of Fallot) may present in shock (tetralogy spells). The most common reason for this decompensation is dehydration. This may occur as a result of exercise or illness.
The cause for these spells is that the left ventricle must have an adequate afterload during systole or its ejection fraction increases. This causes it to accept more blood from the right ventricle via the shunt during diastole. When this happens, as in dehydration, too much blood is diverted from the pulmonary circulation into the systemic circulation. The patient becomes more hypoxic and acidotic, resulting in further decompensation.
PEDS: Children with this defect squat and Valsalva when they feel a spell coming on because squatting causes a rise in peripheral vascular resistance and afterload.
Initial Management
- The most important method of reversing a tetralogy spell is to administer a fluid bolus. PEDS: In children, a 10 to 20 mL/kg fluid bolus is indicated. The fluid bolus restores afterload and corrects the problem.
- If acidosis and hypoxia have been present too long, a dopamine drip at 5 to 20 μg/kg/min may be used temporarily to increase afterload until a compensated state is reached. Too much vasoconstriction causes more acidosis and further decompensation.
Valvular Heart Defects
Valvular heart defects may result from acute myocardial infarction causing papillary muscle dysfunction, spontaneous papillary rupture, or septal rupture (usually 1 to 7 days after a myocardial infarction). A new cardiac murmur in patients with myocardial infarction may indicate the need for urgent cardiac surgery.
Undiagnosed aortic outlet defects such as aortic stenosis, bicuspid aortic valve, or hypertrophic subaortic stenosis may present as sudden death.
Initial Management
- Evaluate patients for cardiac surgery.
- Others may recover spontaneously from a brief episode of exertional syncope. In all syncope patients, listen for a systolic murmur. In such cases, obtain cardiology or surgical consultation urgently.
Kawasaki
Disease
(Mucocutaneous Lymph Node Syndrome)
This disease syndrome is characterized by a prolonged high fever (at least 5 days), erythema of the palms and soles subsequently resulting in desquamation of the digits, stomatitis, conjunctivitis, lymphadenopathy, and a variety of rashes. Arthralgia or arthritis, pyuria or proteinuria, aseptic meningitis, myocarditis, or pericarditis may also occur. Coronary vasculitis may affect as many as 40% of patients with Kawasaki disease with 1% to 2% of patients dying because of coronary vasculitis. Diagnosis is largely based on the constellation of the clinical syndrome findings.
Initial
Management
The inclusion of Kawasaki disease here reflects its potential to cause
myocardial ischemia and infarction in children.
The treatment of primary disease includes administration of salicylates and intravenous immune globulin and is outside the scope of this section.
- Intravenous immunoglobulin stops the process and decreases the risk of coronary disease. This should be given as soon as the diagnosis is clear. Consult pediatric infectious disease if considering this diagnosis and uncertain, then refer for pediatric echocardiography.
- Salicylate therapy is also helpful in suppressing the fever and discomfort.
Stroke (CVA) (Vol
III—NEU2 Treatment of
Stroke)
Patients with an acute focal neurologic deficit suspected of having sustained a stroke (“brain attack”) require a rapid and accurate clinical evaluation including a careful history and a general and neurologic examination. The team must search for an accurate time of onset, keeping in mind that it is defined as the last time that the patient was known to be well. Thus, if a patient awakens with a neurologic deficit, it has to be assumed that the injury occurred when he or she was last known to be asymptomatic. The accurate timing of the injury is essential if thrombolytics are to be considered as part of the treatment plan for the patient.
Key Questions in the Evaluation of a Patient with an Acute Neurologic Deficit
- Is the cause a stroke/TIA or some other diagnosis presenting as an acute neurologic deficit?
- What type of stroke has the patient sustained?
- What is the vascular distribution of the stroke?
- Is the patient a candidate for thrombolytic therapy?
- What immediate evaluation and/or tests are necessary to determine the proper treatment of the patient?
- What early treatments are necessary to minimize the neurologic damage and reduce the associated morbidity associated with the stroke?
Differential diagnosis of a stroke/TIA4:
- Ischemic–atherothrombotic stroke due to a narrowed vessel becoming occluded with a thrombus
- Ischemic-embolic stroke due the embolization of a clot from some source outside of the brain
- Intracranial hemorrhagic stroke due the bleeding of a cerebral vessel bleeding within the brain
- Intracranial hematoma such as an epidural, subdural, or subarachnoid hematoma
- Systemic condition causing a focal neurologic deficit such as hypoglycemia, hyperglycemia, or toxin ingestion
- Rapidly progressive tumors, such as gliomas
- Herpes simplex encephalitis that may show rapid neurologic deterioration
- Todd’s paralysis, a temporary post-ictal paralysis
- Migraine with focal deficit
- Meningitis or encephalitis
- Vasculitis
- Septic embolus
The determination on clinical grounds of the cause for an acute neurologic deficit can be difficult. Some clinical clues include:
- Headache may accompany a stroke, but a severe headache increases the suspicion of a subarachnoid hemorrhage.
- While migraine headache patients may have focal neurologic deficit, for the migraine to be considered a cause of the deficit, the patient should have a migraine history and other conditions must be excluded.
- In general, a hemispheric ischemic stroke does not cause a depressed level of consciousness (LOC) unless it is (1) very large and associated with mass affect, (2) multifocal, or (3) compresses or involves the brain stem and reticular activating system. An intraventricular hemorrhage is more likely to result in a depressed LOC than an ischemic stroke. Thus, when a patient presents with an acute neurologic deficit associated with a depressed LOC, consider the following differential diagnosis4:
-
Large hemispheric stroke with or without mass effect
-
Intraventricular hemorrhage with or without hydrocephalus
-
Cerebellar stroke/bleed/tumor with mass effect and brain stem displacement
-
Intracranial mass (tumor)
-
Post-traumatic concussion or coma
-
Brain stem stroke involving the reticular activating system
-
Meningitis/encephalitis
-
Toxic metabolic encephalopathy
-
Subarachnoid hemorrhage
- A stiff neck (meningismus) may suggest meningitis or subarachnoid hemorrhage.
- An irregular pulse may indicate atrial fibrillation and thus increase the chance of an embolic stroke.
Consider TPA management of acute ischemic strokes in adults if certain specific criteria are met. These include:
-
The patient must be able to receive the TPA within 3 hours of the onset of the acute neurologic deficit.
-
The baseline brain CT must exclude an intracranial hemorrhage and other risk factors to the use of TPA.
-
The patient must be free of contraindications for the use of TPA. (Vol III—NEU2 Treatment of Stroke)
Diagnostic tests to order depend on the clinical situation but may include:
- Blood sugar
- CBC
- Electrolytes
- Brain CT
- Brain MRI
- Lumbar Puncture
Early treatments that may need to be considered to reduce the risk of death or further neurologic damage in a patient who presents with an acute neurologic deficit include:
- Maintaining and supporting an adequate airway and ventilation. Many patients are either hypoxic or are unable to protect their own airway and thus are prone to further neurologic damage or aspiration.
- Increased ICP from brain swelling or edema must be watched for and if present treated.
- Infections such as pneumonia, especially associated with aspiration, or urosepsis must be carefully watched for and treated if present.
- Non-stroke causes of acute neurologic deficit must be sought and treated if present.
Brief Loss of
Consciousness - Syncope
Brief loss of consciousness/syncope is a transient loss of self-awareness or loss of consciousness frequently associated with loss of postural tone that lasts from a few minutes to hours from which the patient spontaneously recovers. While the term syncope is most frequently used in cases when the cause for the loss of consciousness is either due to a brief dysfunction of the vasodepressor cardiovascular refluxes or due to a primary cardiogenic cause, it is frequently difficult to tell during the initial evaluation of a patient if their loss of consciousness fits into one of these categories or has another more specific cause. This discussion does not delineate all potential causes for a patient to have a brief loss of consciousness, (Vol I —Pathway 1 Altered Level of Consciousness) but rather focuses on more common causes to consider.
References
-
ECC Subcommittee, Subcommittees and Task Forces of the American Heart Association. 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010;122(18 suppl 3):S729-S767.
-
Behrman RE, Vaughan VC III, editors. Nelson Textbook of Pediatrics.12th ed. Philadelphia, Pa: WB Saunders Co, 1983
-
Kempe CH, Silver HK, O’Brien D, Fulginiti VA, editors. Current Pediatric Diagnosis and Treatment. 9th ed. Norwalk, Conn: Appleton and Lange, 1987.